Evidence map›Paper›PMID 18787042›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

Rapid recruitment of temporally distinct vascular gene sets by estrogen.

Katrin K Schnoes, Iris Z Jaffe, Lakshmanan Iyer, Alexandra Dabreo, Mark Aronovitz, Brenna Newfell, Ulla Hansen, Giuseppe Rosano, Michael E Mendelsohn

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. bioRxiv : the preprint server for biology · 2024
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  3. Review
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  9. How Gene Networks Can Uncover Novel CVD Players.Current cardiovascular risk reports · 2014
    Article
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  14. Review
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  17. Article
  18. Review
  19. Gender-specific reduction in contraction is associated with increased estrogen receptor expression in single vascular smooth muscle cells of female rat.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2010
    Article
  20. This issue includes more than a conventional discussion of heart disease in women.Journal of cardiovascular translational research · 2009
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Katrin K SchnoesMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 080, Boston, Massachusetts 02111, USA.
Iris Z Jaffe
Lakshmanan Iyer
Alexandra Dabreo
Mark Aronovitz
Brenna Newfell
Ulla Hansen
Giuseppe Rosano
Michael E Mendelsohn
Tufts Medical Center · USBoston University · USIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

NHLBI NIH HHS R01 HL50569
6 · The paper itself

Abstract

Cardiovascular disease is the leading cause of mortality for both men and women in developed countries. The sex steroid hormone estrogen is required for normal vascular physiology. Estrogen functions by binding to intracellular estrogen receptors (ER), ERalpha and ERbeta, ligand-activated transcription factors that are expressed in both vascular endothelial and smooth muscle cells. We recently demonstrated that long-term (8 d) estrogen treatment in vivo in mice recruits distinct vascular gene sets mediated by ERalpha and ERbeta and that the promoters from these gene sets are enriched for binding sites of specific transcription factors, leading to the hypothesis that estrogen initiates a cascade of early transcriptional events that modulate gene expression in the vasculature. Here we test this hypothesis using gene expression profiling to examine initial transcriptional events (2-8 h) mediated by estrogen in blood vessels. Our data reveal that 1) estrogen regulates temporally distinct cascades of vascular gene expression, 2) initially, estrogen-mediated vascular gene repression predominates, 3) the earliest estrogen-recruited gene program is enriched in vascular transcription factors that can interact with binding sites present in estrogen-regulated vascular genes recruited subsequently, and 4) estrogen-regulated genes recruited next have specific functions, including lipid metabolism and cellular growth and proliferation that are potentially important for estrogen's known vascular functions. In summary, estrogen directly and rapidly recruits specific transcriptional factors that then propagate distinct cascades of gene expression. These data define the temporal recruitment of specific vascular genes by estrogen and enable further analysis of the mechanisms by which estrogen directly regulates vascular function.

Indexed as

AnimalsAortaCardiovascular DiseasesEstradiolEstrogen Receptor alphaEstrogen Receptor betaFemaleGene Expression ProfilingHumansKineticsMaleMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalMultigene FamilyEstradiolEstrogen Receptor alphaEstrogen Receptor betaTranscription Factors

Identifiers

PMID18787042
PMCPMC2582543
OpenAlexW2003047888

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.